Morphine differentially affects ventral tegmental and substantia nigra brain reward thresholds☆
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2021, Pharmacology Biochemistry and BehaviorCitation Excerpt :Interestingly, acute morphine fails to affect ICSS in rats implanted with electrode in the SNc. However, repeated daily administration of morphine lead to increases in the ICSS threshold (Nazzaro et al., 1981). Autoradiography binding study revealed that chronic treatment with morphine leads to a significant reduction of [3H]-SCH-23390 and [3H]-spiperone binding to D1 and D2Rs, respectively, in the rat SNc (Spampinato et al., 1988).
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2019, PeptidesCitation Excerpt :For example, both morphine and cocaine facilitated ICSS maintained by electrical stimulation of either the medial forebrain bundle or the paraventricular nucleus; however, morphine was more effective than cocaine to facilitate ICSS of the paraventricular nucleus but less effective than cocaine to facilitate ICSS of the medial forebrain bundle [41]. As another example, morphine facilitated ICSS of the ventral tegmental area but depressed ICSS of the adjacent substantia nigra in rats [42]. MORs are seven-transmembrane domain receptors coupled to the Gαi subunit [43–46].
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2018, Handbook of Behavioral NeuroscienceCitation Excerpt :Harnessing direct targeting of neural substrates governing reward processing, intracranial self-stimulation provided additional support that drugs of abuse evoke both positive and negative effects. Specifically, changes in stimulation intensity necessary to support operant responding (termed “reward threshold”) show that acute administration of virtually any drug abused by humans primes the brain reward system and lowers reward thresholds (Esposito, Motola, & Kornetsky, 1978; Esposito, Perry, & Kornetsky, 1980; Nazzaro, Seeger, & Gardner, 1981; Schaefer & Michael, 1986a). Oppositely, withdrawal from chronic drug use elevates the amount of stimulation intensity needed to support self-stimulation and is interpreted as a deficit in brain reward function (Epping-Jordan, Watkins, Koob, & Markou, 1998; Markou & Koob, 1991; Schaefer & Michael, 1983, 1986b).
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2015, Journal of Substance Abuse TreatmentCitation Excerpt :Furthermore, compared to healthy controls, people in medication-assisted treatment for an opioid use disorder demonstrate a blunted subjective response to non-drug pleasurable activities (Hill et al., 2013; Lubman et al., 2009) and decreased fMRI activity in response to a non-drug reward in the ventral striatum (Gradin, Baldacchino, Balfour, Matthews, & Steele, 2014), a key component of the dopamine mediated brain reward circuitry (Volkow, Wang, Fowler, & Tomasi, 2012). Exposure to drugs of abuse, while initially reinforcing, in part due to an increase in dopamine in the brain reward system (Di Chiara & North, 1992; Tobler, O'Doherty, Dolan, & Schultz, 2007), may lead to alteration of the dopamine response after chronic exposure, (Volkow et al., 2010) resulting in drug rewards having more (and non-drug rewards having less) incentive value (Hyman, Malenka, & Nestler, 2006; Koob & Le Moal, 2001; Nazzaro, Seeger, & Gardner, 1981; Robinson & Berridge, 1993). Medication-assisted treatment decreases illicit opioid use (Mattick, Kimber, Breen, & Davoli, 2008), but does not appear to ameliorate the alteration in reward processing seen in drug dependent individuals.
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This research was supported, in part, by NIDA grant DA-01560 to Dr. E.L. Gardner and NIDA grant DA-02089 to Dr. W.H. Bridger. Dr. T.F. Seeger was supported by NIH training grant GM-07260 and by a Sue Golding Stipend from the Albert Einstein College of Medicine. Development of the ICSS paradigm was supported, in part, by the U.S. Air Force (Aeromedical Division) under Research Project 6893-02-039 to Dr. E.L. Gardner. The naloxone was generously donated by Endo Laboratories, Inc. We thank Dr. George Alheid for writing the computer programs for the on-line data analysis system used with the ICSS paradigm, and Marie Elbert for assistance with the histological material.
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Present address: Department of Pharmacology, University of Massachusetts Medical Center, Worcester, MA 01605.